Effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on incidence and progress of posterior subcapsular opacities (PSO) associated with genetically influenced retinal degeneration are being studied in pink-eyed Royal College of Surgeons (RCS)rats, in which rod photoreceptor outer segment debris accumulates secondarily to a phagocytic defect in retinal pigmented epithelium (RPE). Peroxidation in polyunsaturated fatty acids (PUFA) in debris leads to water-soluble toxic aldehydes, detectable in the vitreous and toxic to lens cells and membranes. Dystrophic rats fed a natural ingredient diet (NH-07) were highly sensitive to retina light damage, beginning at an intensity of 10 to 40 lux, and 27 percent of the rats developed mature cataracts by five to 12 months. Rhodopsin bleaching is essential for retina light damage and PSO. In vitro, free retinaldehyde has been shown to be a photosensitizer to generate singlet oxygen, an extremely damaging oxidant for both lipids and proteins, and this may also occur in vivo in the RCS disease. In RCS rats reared at 10 to 40 lux, a purified diet (AIN- 76A) fortified with antioxidatns (0.4 percent beta-carotene + 0.01 percent BHT) prevented PSO and mature cataracts. A diet containing additional antioxidants (1000 mg/KG diet of vitamin C and 150 mg/Kg vitamin E) retarded retinal degeneration during the time the cataracts would have had their onset (23 to 55 postnatal days) if NIH-07 had been fed. Higher concentrations of vitamin E did not show additional retardation of retinal degeneration. More intense environmental lighting increased incidence of bilateral mature cataracts (BMC) in rats fed NIH-07. BMC incidence was five percent in rats reared in cyclic light of 10 to 40 lux, but was 25 percent in constant light of 100 lux, 70 percent at 270 lux, and 100 percent in 65-day- old rats given 48 hours at 7500 lux intensity. After lengthy or intense light, the lens showed disturbed meridional rows of lens epithelial cells and posterior nucleated cells, pointing to proliferation of germinative zone cells from DNA damage. At low illumination, damage can be repaired. Stationary cataracts are seen, and BMC are rare. Results are consistent with the hypothesis of PSC causation by DNA damage to lens epithelial cells. Agents that can have this affect include peroxidation products of PUFA, short wavelength radiation (UV, X-rays, beta and gamma rays) and chemical mutagens such as N- methyl-N-nitrosourea (MNU). Normal albino rats injected with MNU, at a concentration and dosage sufficient to cause breast cancer, developed BMC by five months of age. These cataracts were PSC of a more severe nature than ever seen in RCS rats (exposed to excessive light), with abnormal nucleated lens epithelial cells not only at the posterior pole but encircling the lens. MNU may thus provide an experimental rat cataract model.